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Vitamin C Inhibits Endothelial Cell Apoptosis in Congestive Heart Failure
Open accessAbstract
Background Proinflammatory cytokines like tumor necrosis factor-α and oxidative stress induce apoptotic cell death in endothelial cells (ECs). Systemic inflammation and increased oxidative stress in congestive heart failure (CHF) coincide with enhanced EC apoptosis and the development of endothelial dysfunction. Therefore, we investigated the effects of antioxidative vitamin C therapy on EC apoptosis in CHF patients. Methods and Results Vitamin C dose dependently suppressed the induction of EC apoptosis by tumor necrosis factor-α and angiotensin II in vitro as assessed by DNA fragmentation, DAPI nuclear staining, and MTT viability assay. The antiapoptotic effect of vitamin C was associated with reduced cytochrome C release from mitochondria and the inhibition of caspase-9 activity. To assess EC protection by vitamin C in CHF patients, we prospectively randomized CHF patients in a double-blind trial to vitamin C treatment versus placebo. Vitamin C administration to CHF patients markedly reduced plasma levels of circulating apoptotic microparticles to 32±8% of baseline levels, whereas placebo had no effect (87±14%, P <0.005). In addition, vitamin C administration suppressed the proapoptotic activity on EC of the serum of CHF patients ( P <0.001). Conclusions Administration of vitamin C to CHF patients suppresses EC apoptosis in vivo, which might contribute to the established functional benefit of vitamin C supplementation on endothelial function.
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“Vitamin C has been found to reduce the cholesterol level in patients with hypercholesterolemia (Rossig et al. 2001)”
From Reactive Oxygen Species, Toxicity, Oxidative Stress, and Antioxidants: Chronic Diseases and Aging (2023) · cites this paper as Rossig et al. 2001
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Metadata
- Authors
- Rössig, L., Hoffmann, J., Hugel, B., Mallat, Z., Haase, A., Freyssinet, J.-M., Tedgui, A., Aicher, A., Zeiher, A. M., & Dimmeler, S.
- Affiliations
- From Molecular Cardiology, Department of Internal Medicine IV, University of Frankfurt, Germany (L.R., J.H., A.H., A.A., A.M.Z., S.D.); INSERM U141, IFR “Circulation,” Hôpital Lariboisière, Paris, France (Z.M., A.T.); and Institut d’Hématologie et d’Immunologie, Faculté de Médecine, Université Louis Pasteur, Strasbourg, France (B.H., J.-M.F.).
- Goethe University Frankfurt (DE)
- Venue
- Circulation
- Published
- 2001-10-30
- Volume
- 104
- Issue
- 18
- Pages
- 2182-2187
- ISSN
- 0009-7322 (ISSN-L)
- 1524-4539
- OpenAlex
- W2170212513
- Cited by
- 182
- References
- 29
- Citations by year
- 2026: 1 · 2024: 1 · 2023: 4 · 2022: 5 · 2021: 5 · 2020: 4 · 2019: 4 · 2018: 3 · 2017: 2 · 2016: 1 · 2015: 6 · 2014: 15 · 2013: 11 · 2012: 9
- FWCI
- 10.72
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Circulation (publishedVersion)
- PubMed (publishedVersion)
- Nottingham Trent University's Institutional Repository (Nottingham Trent Repository) (acceptedVersion)
- Funders
- Boehringer Ingelheim Fonds
- Deutsche Forschungsgemeinschaft (SFB 553)
- Topics
- Health Sciences › Nursing › Nutrition and Dietetics › Vitamin C and Antioxidants Research
- Health Sciences › Medicine › Physiology (medical) › Nitric Oxide and Endothelin Effects
- Health Sciences › Medicine › Biochemistry (medical) › Antioxidant Activity and Oxidative Stress
- Keywords
- vitamin C, congestive heart failure, endothelial cell apoptosis, endothelial dysfunction, TNF-α, angiotensin II, oxidative stress, systemic inflammation, cytochrome c release, caspase-9, antioxidant therapy
- MeSH terms
- Administration, Oral, Adult, Aged, Angiotensin II, Ascorbic Acid, Cell Survival, Cells, Cultured, Dose-Response Relationship, Drug, Drug Administration Schedule, Endothelium, Vascular, Enzyme Inhibitors, Female, Heart Failure, Humans, Injections, Intravenous, Male, Middle Aged, Prospective Studies, Tumor Necrosis Factor-alpha, Biomarkers, Apoptosis, Thiobarbituric Acid Reactive Substances, Oxidative Stress
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